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Irisflorentin

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-I3005

  • Specification : 98%

  • CAS number : 41743-73-1

  • Formula : C20H18O8

  • Molecular Weight : 386.35

  • PUBCHEM ID : 170569

  • Volume : 25mg

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Catalogue Number

BF-I3005

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

386.35

Appearance

White crystalline powder

Botanical Source

Belamcanda chinensis,Iris dichotoma,Iris leptophylla

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC(=CC(=C1OC)OC)C2=COC3=CC4=C(C(=C3C2=O)OC)OCO4

Synonyms

Irisflorentin/3',4',5',5-tetramethoxy-6,7-methylenedioxyisoflavone/irisflorentine/9-methoxy-7-(3,4,5-trimethoxy-phenyl)-[1,3]dioxolo[4,5-g]chromen-8-one/9-Methoxy-7-(3,4,5-trimethoxyphenyl)-8H-[1,3]dioxolo[4,5-g]chromen-8-one/9-Methoxy-7-(3,4,5-trimethoxyphenyl)-8H-1,3-dioxolo[4,5-g][1]benzopyran-8-one/8H-1,3-Dioxolo[4,5-g][1]benzopyran-8-one, 9-methoxy-7-(3,4,5-trimethoxyphenyl)-/N1426/9-Methoxy-7-(3,4,5-trimethoxyphenyl)-8H-1,3-dioxolo(4,5-g)(1)benzopyran-8-one/5,3',4',5'-Tetramethoxy-6,7-methylenedioxyisoflavone/8H-1,3-Dioxolo(4,5-g)(1)benzopyran-8-one, 9-methoxy-7-(3,4,5-trimethoxyphenyl)-

IUPAC Name

9-methoxy-7-(3,4,5-trimethoxyphenyl)-[1,3]dioxolo[4,5-g]chromen-8-one

Density

1.3±0.1 g/cm3

Solubility

Methanol

Flash Point

250.5±30.2 °C

Boiling Point

569.1±50.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C20H18O8/c1-22-13-5-10(6-14(23-2)18(13)24-3)11-8-26-12-7-15-19(28-9-27-15)20(25-4)16(12)17(11)21/h5-8H,9H2,1-4H3

InChl Key

RISXUTCDCPHJFQ-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:41743-73-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

25654487

Abstract

Irisflorentin is an isoflavone component derived from the roots of Belamcanda chinensis (L.) DC. In traditional Chinese medicine, this herb has pharmacological properties to treat inflammatory disorders. Dendritic cells (DCs) are crucial modulators for the development of optimal T-cell immunity and maintenance of tolerance. Aberrant activation of DCs can induce harmful immune responses, and so agents that effectively improve DC properties have great clinical value. We herein investigated the effects of irisflorentin on lipopolysaccharide (LPS)-stimulated maturation of mouse bone marrow-derived DCs in vitro and in the contact hypersensitivity response (CHSR) in vivo. Our results demonstrated that treatment with up to 40 μM irisflorentin does not cause cellular toxicity. Irisflorentin significantly lessened the proinflammatory cytokine production (tumor necrosis factor-α, interleukin-6, and interleukin-12p70) by LPS-stimulated DCs. Irisflorentin also inhibited the expression of LPS-induced major histocompatibility complex class II and costimulatory molecules (CD40 and CD86) on LPS-stimulated DCs. In addition, irisflorentin diminished LPS-stimulated DC-elicited allogeneic T-cell proliferation. Furthermore, irisflorentin significantly interfered with LPS-induced activation of IκB kinase, c-Jun N-terminal kinase, and p38, as well as the nuclear translocation of NF-κB p65. Subsequently, treatment with irisflorentin obviously weakened 2,4-dinitro-1-fluorobenzene-induced delayed-type hypersensitivity. These findings suggest new insights into the role of irisflorentin as an immunotherapeutic adjuvant through its capability to modulate the properties of DCs.

Title

Irisflorentin Modifies Properties of Mouse Bone Marrow-Derived Dendritic Cells and Reduces the Allergic Contact Hypersensitivity Responses

Author

Ru-Huei Fu 1 , Chia-Wen Tsai, Rong-Tzong Tsai, Shih-Ping Liu, Tzu-Min Chan, Yu-Chen Ho, Hsin-Lien Lin, Yue-Mi Chen, Huey-Shan Hung, Shao-Chih Chiu, Chang-Hai Tsai, Yu-Chi Wang, Woei-Cherng Shyu, Shinn-Zong Lin

Publish date

2015

PMID

25705584

Abstract

Parkinson’s disease (PD) is a degenerative disorder of the central nervous system that is characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta as well as motor impairment. Aggregation of α-synuclein in neuronal cells plays a key role in this disease. At present, therapeutics for PD provides moderate symptomatic benefits, but it is not able to delay the development of the disease. Current efforts toward the treatment of PD are to identify new drugs that slow or arrest the progressive course of PD by interfering with a disease-specific pathogenetic process in PD patients. Irisflorentin derived from the roots of Belamcanda chinensis (L.) DC. is an herb which has been used for the treatment of inflammatory disorders in traditional Chinese medicine. The purpose of the present study was to assess the potential for irisflorentin to ameliorate PD in Caenorhabditis elegans models. Our data reveal that irisflorentin prevents α-synuclein accumulation in the transgenic Caenorhabditis elegans model and also improves dopaminergic neuron degeneration, food-sensing behavior, and life-span in a 6-hydroxydopamine-induced Caenorhabditis elegans model, thus indicating its potential as a anti-parkinsonian drug candidate. Irisflorentin may exert its effects by promoting rpn-3 expression to enhance the activity of proteasomes and down-regulating egl-1 expression to block apoptosis pathways. These findings encourage further investigation on irisflorentin as a possible potent agent for PD treatment.

Title

Irisflorentin Improves α-Synuclein Accumulation and Attenuates 6-OHDA-induced Dopaminergic Neuron Degeneration, Implication for Parkinson's Disease Therapy

Author

Yue-Mi Chen 1 , Shih-Ping Liu 2 , Hsin-Lien Lin 1 , Ming-Chia Chan 1 , Yen-Chuan Chen 1 , Yu-Ling Huang 1 , Min-Chen Tsai 1 , Ru-Huei Fu 2

Publish date

2015

PMID

24740875

Abstract

Irisflorentin, a naturally occurring isoflavone, is an abundant active constituent in Rhizoma Belamcandae. Although some chemical studies have been reported, pharmacological actions of irisflorentin are not well studied. In this study, we demonstrate the anti-inflammatory activity of irisflorentin in lipopolysaccharides (LPS)-stimulated RAW 264.7 macrophages. Irisflorentin markedly reduces the transcriptional and translational levels of inducible nitric oxide synthase (iNOS) as well as the production of NO. Furthermore, it also significantly inhibits TNF-α, IL-1β and IL-6 at both the transcriptional and translational levels. These effects mainly act via ERK1/2 – and p38-mediated the activator protein-1 (AP-1) rather than the nuclear factor-κB (NF-κB) pathway. Thus, our study elucidates the anti-inflammatory mechanism of irisflorentin in LPS-activated RAW 264.7 macrophages.

KEYWORDS

AP-1 pathway; Irisflorentin; LPS; RAW 264.7 macrophages; anti-inflammatory.

Title

Suppressive Effects of Irisflorentin on LPS-induced Inflammatory Responses in RAW 264.7 Macrophages

Author

Yuan Gao 1 , Lei Fang 1 , Fen Liu 1 , Chuanjie Zong 1 , Runlan Cai 1 , Xi Chen 1 , Yun Qi 2

Publish date

2014 Aug


Description :

Irisflorentin improves α-synuclein accumulation and attenuates 6-OHDA-induced dopaminergic neuron degeneration, implication for Parkinson's disease therapy. PUMID/DOI:25705584 Biomedicine (Taipei). 2015;5(1):4. Epub 2015 Feb 2. Parkinson's disease (PD) is a degenerative disorder of the central nervous system that is characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta as well as motor impairment. Aggregation of α-synuclein in neuronal cells plays a key role in this disease. At present, therapeutics for PD provides moderate symptomatic benefits, but it is not able to delay the development of the disease. Current efforts toward the treatment of PD are to identify new drugs that slow or arrest the progressive course of PD by interfering with a disease-specific pathogenetic process in PD patients. Irisflorentin derived from the roots of Belamcanda chinensis (L.) DC. is an herb which has been used for the treatment of inflammatory disorders in traditional Chinese medicine. The purpose of the present study was to assess the potential for Irisflorentin to ameliorate PD in Caenorhabditis elegans models. Our data reveal that Irisflorentin prevents α-synuclein accumulation in the transgenic Caenorhabditis elegans model and also improves dopaminergic neuron degeneration, food-sensing behavior, and life-span in a 6-hydroxydopamine-induced Caenorhabditis elegans model, thus indicating its potential as a anti-parkinsonian drug candidate. Irisflorentin may exert its effects by promoting rpn-3 expression to enhance the activity of proteasomes and down-regulating egl-1 expression to block apoptosis pathways. These findings encourage further investigation on Irisflorentin as a possible potent agent for PD treatment. Irisflorentin modifies properties of mouse bone marrow-derived dendritic cells and reduces the allergic contact hypersensitivity responses. PUMID/DOI:25654487 Cell Transplant. 2015;24(3):573-88. Irisflorentin is an isoflavone component derived from the roots of Belamcanda chinensis (L.) DC. In traditional Chinese medicine, this herb has pharmacological properties to treat inflammatory disorders. Dendritic cells (DCs) are crucial modulators for the development of optimal T-cell immunity and maintenance of tolerance. Aberrant activation of DCs can induce harmful immune responses, and so agents that effectively improve DC properties have great clinical value. We herein investigated the effects of Irisflorentin on lipopolysaccharide (LPS)-stimulated maturation of mouse bone marrow-derived DCs in vitro and in the contact hypersensitivity response (CHSR) in vivo. Our results demonstrated that treatment with up to 40 μM Irisflorentin does not cause cellular toxicity. Irisflorentin significantly lessened the proinflammatory cytokine production (tumor necrosis factor-α, interleukin-6, and interleukin-12p70) by LPS-stimulated DCs. Irisflorentin also inhibited the expression of LPS-induced major histocompatibility complex class II and costimulatory molecules (CD40 and CD86) on LPS-stimulated DCs. In addition, Irisflorentin diminished LPS-stimulated DC-elicited allogeneic T-cell proliferation. Furthermore, Irisflorentin significantly interfered with LPS-induced activation of IκB kinase, c-Jun N-terminal kinase, and p38, as well as the nuclear translocation of NF-κB p65. Subsequently, treatment with Irisflorentin obviously weakened 2,4-dinitro-1-fluorobenzene-induced delayed-type hypersensitivity. These findings suggest new insights into the role of Irisflorentin as an immunotherapeutic adjuvant through its capability to modulate the properties of DCs. Suppressive effects of irisflorentin on LPS-induced inflammatory responses in RAW 264.7 macrophages. PUMID/DOI:24740875 Exp Biol Med (Maywood). 2014 Apr 16;239(8):1018-1024. Irisflorentin, a naturally occurring isoflavone, is an abundant active constituent in Rhizoma Belamcandae. Although some chemical studies have been reported, pharmacological actions of irisflorentin are not well studied. In this study, we demonstrate the anti-inflammatory activity of irisflorentin in lipopolysaccharides (LPS)-stimulated RAW 264.7 macrophages. Irisflorentin markedly reduces the transcriptional and translational levels of inducible nitric oxide synthase (iNOS) as well as the production of NO. Furthermore, it also significantly inhibits TNF-α, IL-1β and IL-6 at both the transcriptional and translational levels. These effects mainly act via ERK1/2?- and p38-mediated the activator protein-1 (AP-1) rather than the nuclear factor-κB (NF-κB) pathway. Thus, our study elucidates the anti-inflammatory mechanism of irisflorentin in LPS-activated RAW 264.7 macrophages.